Acrolein-induced cell death in human alveolar macrophages

Li Li, Raymond F. Hamilton, David E. Taylor, Andrij Holian

Research output: Contribution to journalArticlepeer-review

Abstract

Acrolein is an environmental air pollutant that is known to suppress respiratory host defense against infections. The mechanism of the decrease in host defense is not yet clear. In this study, the effects of acrolein on human alveolar macrophages and their function were examined. Acrolein caused dose-dependent cytotoxicity to alveolar macrophages as demonstrated by the induction of apoptosis and necrosis. In addition, at lower doses, acrolein caused induction of heme oxygenase 1 protein; however, stress protein 72 (SP72) was not induced. These findings demonstrated that acrolein caused a dose-dependent selective induction of a stress response, apoptosis, and necrosis in human alveolar macrophages. Macrophage function was assessed by release of cytokines in response to endotoxin stimulation. Acrolein caused a dose-dependent inhibition of release of IL-1β, TNF-α, and IL-12. The inhibition of cytokine release and cytotoxicity to alveolar macrophages may in part be responsible for acrolein-induced immunosuppression of the lung.

Original languageEnglish
Pages (from-to)331-339
Number of pages9
JournalToxicology and Applied Pharmacology
Volume145
Issue number2
DOIs
StatePublished - Aug 1997

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